Progress of diagnosis and treatment of precancerous pathological lesions of mammary cancer / 中国中西医结合杂志

Prevention and treatment of mammary cancer has been taken into great account recently. "Mutistage developing mode" provides the basis for interrupting and reversing precancerous changes. Traditional Chinese medicine (TCM) has shown effects on precancerous changes through inhibiting angiogenesis, promoting apoptosis, modulating endocrine system and restraining oncogene expression. It was stressed in this review that TCM should study the precancerous change of mammary cancer from the aspects of recognizing the essence of precancerous changes of mammary cancer, formulating the standard of TCM diagnosis and treatment, widening the aim of treatment, and focusing on the mechanism of Chinese herbal medicine in intervening it.

Clinical research on relationship between angiogensis and TCM syndrome type of cyclomastopathy / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To study the relationship between angiogensis and TCM Syndrome type of cyclomastopathy (CMP) to investigate the objective standardization of TCM Syndrome diagnosis of the disease.</p><p><b>METHODS</b>One hundred and forty patients with CMP were divided into three groups according to TCM syndrome typing. The pathological type, grade and expressions of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF) and microvascular density (MVD) in mammary biopsy were observed.</p><p><b>RESULTS</b>The expressions of VEGF, bFGF and MVD was different in CMP patients of different TCM types and pathological grades (P < 0.05). The proportion of atypical proliferation, the count of MVD and the expression of VEGF and bFGF were higher in patients of phlegm and stasis type than those in Gan stagnation caused Qistagnation type and Chong and Ren meridians disorder type.</p><p><b>CONCLUSION</b>TCM Syndrome type of CMP patients is related with vascular activity and grade of angiogensis. The pathological characteristics of mammary tissue and expression of VEGF, bFGF and MVD can be regarded as the objective indexes of TCM typing and clinical efficacy evaluation for CMP.</p>

Rosiglitazone inhibits atherosclerosis in apolipoprotein E-knockout mice / 中华心血管病杂志

<p><b>OBJECTIVE</b>To study the effect of rosiglitazone on atherosclerosis and potential mechanism in ApoE-knockout mice.</p><p><b>METHODS</b>Thirty-two 6-week-old ApoE-knockout mice were used as atherosclerosis model in two groups: rosiglitazone group (n = 18) and control group (n = 14). Each group contained equal numbers of male and female mice. All mice were fed with normal chow diet. In addition to normal diet, rosiglitazone group received rosiglitazone 17 mg/kg of body weight/day. Venous bloods were collected for plasma glucose and lipid analysis, and aorta were prepared for morphologic and immunohistochemical analysis after 14 weeks. Aortic root (1 cm) was cut and prepared for paraffin slice. The histomorphometric analysis of atherosclerotic lesion was performed by means of HE; positive percentage of macrophage cell and tumor necrosis factor-alpha were measured by means of immunohistochemistry in cross section. The ratio of lesion/aortic wall surface in the rest aorta was measured by means of Sudan IV staining in longitudinal section.</p><p><b>RESULTS</b>The amount of fatty streak in rosiglitazone group was significantly greater than that of control group; the gross number of lesions and the number of fibrous plaque and atheromatous plaque were similar in two groups. There were no differences in percentage of lesions in cross section in two groups. Rosiglitazone could significantly reduce the extend of atherosclerosis of longitudinal section, decrease the amount of macrophage cell and the level of tumor necrosis factor-alpha in lesions. The plasma glucose was normal and similar in two groups, and total cholesterol, LDL-cholesterol and triglyceride were significantly higher in rosiglitazone group.</p><p><b>CONCLUSION</b>Rosiglitazone suppresses the expression of tumor necrosis factor-alpha, reduces the number of macrophage cell in lesion, and inhibits the development of atherosclerosis.</p>